{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T04:05:23Z","timestamp":1792123523664,"version":"4.4.0"},"reference-count":92,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2017,8,11]],"date-time":"2017-08-11T00:00:00Z","timestamp":1502409600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004628","name":"MedImmune","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004628","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1 TR00043"],"award-info":[{"award-number":["UL1 TR00043"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2017,11]]},"abstract":"Summary<\/jats:title>Background<\/jats:title>Atopic dermatitis (AD<\/jats:styled-content>), psoriasis (PS<\/jats:styled-content>), and contact dermatitis (CD<\/jats:styled-content>) are common skin diseases, characterized by barrier disruption and systemic inflammation, with unique epidermal signatures and common inflammatory pathways identified by transcriptomic profiling. This study profiled proteomic signatures in serum from subjects with AD<\/jats:styled-content>, PS<\/jats:styled-content>, and CD<\/jats:styled-content> compared with healthy controls (HC<\/jats:styled-content>).<\/jats:p><\/jats:sec>Objective<\/jats:title>Identify unique proteomic signatures to distinguish between inflammatory diseases with similar epidermal disruption and overlapping epithelial inflammation.<\/jats:p><\/jats:sec>Methods<\/jats:title>Sera from 20 subjects with moderate to severe AD<\/jats:styled-content>, 10 subjects with CD<\/jats:styled-content>, 12 subjects with moderate to severe PS<\/jats:styled-content>, 10 subjects with both AD<\/jats:styled-content> and CD<\/jats:styled-content>, and 10 HC<\/jats:styled-content> with no history of skin disease was analysed using high\u2010throughput proteomic analysis that detects expression of 1129 protein targets. Protein expression was compared between disease and HC<\/jats:styled-content>, and across diseases for statistical significance (fold change\u22651.5 and false discovery rate\u22640.05), to identify unique proteomic signatures for each disease.<\/jats:p><\/jats:sec>Results<\/jats:title>Complement C5A anaphylatoxin (C5A), lipopolysaccharide binding protein (LBP<\/jats:styled-content>), C\u2010reactive protein (CRP<\/jats:styled-content>), ILT<\/jats:styled-content>\u20104, C\u2010C motif ligand 18 (PARC<\/jats:styled-content>), and sialic acid\u2010binding Ig\u2010like lectin 14 (SIG<\/jats:styled-content>14) were significantly modulated in all three diseases compared with HC<\/jats:styled-content>. We identified unique signatures for AD<\/jats:styled-content> (Immunoglobulin E (IgE), thymus\u2010 and activation\u2010regulated chemokine (TARC<\/jats:styled-content>) and macrophage\u2010derived chemokine (MDC<\/jats:styled-content>)), CD<\/jats:styled-content> (10 proteins), and PS<\/jats:styled-content> (kynureninase (KYNU<\/jats:styled-content>)). Proteomic profiling in subjects with both AD<\/jats:styled-content> and CD<\/jats:styled-content> identified additional dysregulated proteins compared with subjects with either condition alone, indicating an exacerbated inflammation reaction.<\/jats:p><\/jats:sec>Conclusions and Clinical Relevance<\/jats:title>Unique sera proteomic signatures may distinguish between inflammatory skin diseases despite similar epidermal barrier disruption and epithelial inflammation. This may provide insight into disease pathogenesis, diagnosis, and therapeutic intervention in difficult\u2010to\u2010treat subjects.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.12979","type":"journal-article","created":{"date-parts":[[2017,7,13]],"date-time":"2017-07-13T15:05:16Z","timestamp":1499958316000},"page":"1456-1467","source":"Crossref","is-referenced-by-count":57,"title":["Identification of unique proteomic signatures in allergic and non\u2010allergic skin disease"],"prefix":"10.1111","volume":"47","author":[{"given":"J.","family":"Wang","sequence":"first","affiliation":[{"name":"MedImmune, LLC Gaithersburg MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Su\u00e1rez\u2010Fari\u00f1as","sequence":"additional","affiliation":[{"name":"Department of Dermatology and the Laboratory for Inflammatory Skin Diseases Icahn School of Medicine at Mount Sinai Medical Center New York NY USA"},{"name":"Department of Population Health Science and Policy Icahn School of Medicine at Mount Sinai Medical Center New York NY USA"},{"name":"Icahn Institute for Genomics and Multiscale Biology at Mount Sinai Icahn School of Medicine at Mount Sinai New York NY USA"},{"name":"Laboratory for Investigative Dermatology Rockefeller University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Estrada","sequence":"additional","affiliation":[{"name":"Department of Dermatology and the Laboratory for Inflammatory Skin Diseases Icahn School of Medicine at Mount Sinai Medical Center New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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